While much research has been done in an attempt to understand the neurophysiological mechanisms underlying epileptiform activity in the mature nervous system, comparatively few attempts have been made to study epileptogenesis in he immature brain. Clinical observations support the premise that the epileptogenic properties of the central nervous system vary dramatically during development. It has been postulated tha the hippocampus in one area of the immature brain which is unusually susceptible to seizures. In preliminary experiments presented here epileptiform activity was compared between immature and mature hippocampal slices, during exposure to the convulsant, penicillin. Extracellular field potential recordings from the CA3 region demonstrated that: 1) mature CA3 neurons are able to generate spontaneous and evoked epileptiform bursts, commonly called interictal spikes, 2) slices from 9-19 day old rats also produce interictal spikes, however, these epileptiform bursts are followed by 0prolonges afterdischarges, which often approached a 30 sec duration. Field recordings fromt he CA3 pyramidal cell body layer of penicillin-treated, 9-19 day old rat slices show that a large prolonged negative field potential is associated with the afterdischarge. Intracellular recordings from immature and mature slices reveal that they both produce paroxysmal depolarization shifts (PDS) which are coincident with the field interictal spikes. However, whereas the PDS in mature CA3 pyramidal cells is followed by a prolonged afterhyperpolarization, the PDS in 9-19 day old CA3 neurons is followed by a slow depolarizing after-potential (DAP). Often the DAP is prolonged and associated with an afterdischarge. Intracellularly, the afterdishcarge consists of large, slow, rhythmic, depolarizing potentials, which ride on the envelope of the DAP. Since the slow negative field potentials and depolarizing afterpotentials recordings in the immature hippocampal slices are associated with their ability to undergo prolonged discharges, it is possible that these potentials contribute in a major way to the susceptibility of the immature hippocampus to seizures. Accordingly, these potentials deserve to be closely examined. The research, proposed here, will attempt to determine the origins of these two potentials.